We have previously reported on the presence of proenzymes and inhibito
rs of the contact system in ascitic fluid. Malignancy-related ascites
was also found to contain both high and low molecular weight kininogen
(HK and LK). On this basis we have studied a possible activation of t
he contact system in ascites. Generation of amidolytic activity toward
s the chromogenic substrate S-2302 after incubation with dextran sulph
ate (DXS), was found in ascites from patients with gastrointestinal ca
ncer, but not in ascites from patients with benign liver disease. It i
s concluded that malignancy-related ascites allows contact activation
to take place, while benign ascites does not. This activation process,
generating bradykinin, could possibly be of relevance to the mechanis
m of ascites generation. Plasma samples from patients with ascites wer
e also tested in relation to activation of the contact system. Activat
ion was evaluated by immunoblotting, studying the disappearance of int
act HK after the initiation of activation with different concentration
s of DXS. In control plasma, activation took place at low concentratio
ns of DXS (25 - 50 mu g/ml). In plasma samples from patients with mali
gnancy-related or benign ascites, contact activation was depressed. In
some samples concentrations of DXS up to 1 mg/ml, were not able to ac
tivate the contact system at all. Concentrations of proenzymes and rel
evant inhibitors in the contact system, HK and total protein were also
determined. We found the concentration of prekallikrein to be positiv
ely correlated with the degree of activation. Concentrations of inhibi
tors such as C1-inhibitor, did not show any correlation with activatio
n.